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CeO 2 nanoparticles (CNPs) as effective ROS scavengers exhibit potent antioxidant activity. In this study the effect of CNPs investigated was on HO-1, NQO1, and GCLC expression in the streptozotocin (STZ)-induced diabetic rats. Twenty-four male Wistar rats were divided into 4 groups: controls did not receive any treatment; diabetic rats received STZ (60 mg/kg daily); CNPs group received CNPs 30 mg/kg daily for 2 weeks; and rats in STZ + CNPs group received CNPs 30 mg/kg daily for 2 weeks following STZ injection. Oxidative stress was evaluated by measurement of total antioxidant capacity (TAC) and total oxidative status (TOS levels). HO-1, NQO1, and GCLC expression was measured using quantitative real-time PCR. Following STZ injection, significant lower levels of TAC and higher levels of TOS were observed. CNPs could alleviate deleterious effects of diabetes through the enhancement of TAC levels and a significant decline in TOS levels. HO-1, NQO1, and GCLC expression in the diabetic rats were lower than controls. HO-1, NQO1, and GCLC was upregulated in the diabetic rats treated with CNPs. There were significant correlations between NQO1 and GCLC, NQO1 and HO-1, and between HO-1 and GCLC expression. Moreover, Nrf2 was associated with NQO1, GCLC, and HO-1 expression. CNPs as Nrf2 upregulator confer protection against oxidative stress in the testes of STZ-induced diabetic rats by upregulating HO-1, GCLC, and NQO1 cytoprotective genes.

Introduction: Diabetes mellitus is a major chronic metabolic disorder that induces memory and learning impairment. Herein, we investigated the protective effects of cerium oxide nanoparticles (CeO2) against streptozotocin (STZ)-induced memory impairment and antioxidant capacity in the diabetic rats. Methods: Adult male Wistar rats were assigned into the control, STZ, CeO2 and STZ plus CeO2 groups. Diabetes was induced using STZ and next CeNPs (60mg/kg) was administered for 14 constitutive days. The day after the last administration, spatial memory was assessed using the Morris water maze (MWM). Ultimately, the level of total antioxidant capacity (TAC) was investigated. Results: Our results showed that STZ significantly decreased the spatial memory and CeO2 could compensate for these changes. Furthermore, TAC increased following administration of CeO2 in the diabetic rats. Conclusion: The results of this study suggest that CeO2 seems to be able to improve STZ-induced neurotoxicity in the rats. [ABSTRACT FROM AUTHOR]

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